American Association for Cancer Research

Continuing Medical Education (CME)

RAS Oncogenes: From Biology to Therapy 2014

ACCREDITATION STATEMENT

The American Association for Cancer Research (AACR) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education activities for physicians.

CREDIT DESIGNATION STATEMENT

The AACR has designated this live activity for a maximum of 16.5 AMA PRA Category 1 Credit(s)TM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Credit certification for individual sessions may vary, dependent upon compliance with the ACCME Accreditation Criteria. The final number of credits may vary from the maximum number indicated above.

CLAIMING (CME) CREDIT

Physicians and other health care professionals seeking AMA PRA Category 1 Credit(s)TM for this live continuing medical education activity must complete the CME Request for Credit Survey, below, by Thursday, April 10, 2014. Certificates will only be issued to those who complete the survey. Your CME certificate will be sent to you via email after the completion of the activity.

STATEMENT OF EDUCATIONAL NEED, TARGET AUDIENCE, AND LEARNING OBJECTIVES

RAS genes are often mutated in human cancers and remarkable discoveries regarding how RAS proteins function as key regulators of signal transduction and drivers of oncogenesis have emerged over the past three decades. Approximately 30 percent of human tumors harbor mutations in one of the three RAS isoforms: KRAS, NRAS, and HRAS. However, past attempts to target the proteins encoded by RAS genes have been unsuccessful and tumors with RAS mutations have often been excluded from treatment with targeted therapies. Thus, despite intensive efforts by the pharmaceutical industry, it has been challenging to translate findings into clinically effective anti-RAS therapies, and RAS has been widely perceived as “undruggable.”

However, recent genomewide sequencing studies performed in search of new targets revealed that RAS and its key effectors (BRAF and PIK3CA) are the only oncogenes mutated beyond single digit frequencies in the cancers that comprise three of the top four causes of death in the U.S. (lung, colon, and pancreatic cancer). This has prompted renewed interest in targeting RAS, including the recent US National Cancer Institute announcement of a RAS “megaproject” to support such efforts. Additionally, recent research on KRAS suggests that it may be possible to block mutant KRAS proteins while leaving normal proteins unharmed.

Given the prominent role of RAS in human cancers, there is a need to educate physicians on the most recent developments in RAS research as the push for targeted therapies intensifies. This conference will cover a range of the topics from RAS regulation to the basic biology and therapeutics of RAS effectors. It will also address systems approaches to RAS biology, models of RAS-driven cancers, and RAS targeting in cancer treatment.

The primary focus of this AACR Special Conference will be to discuss both the exciting progress and the many still-unresolved issues that will affect how these discoveries can be leveraged. This conference will bring together academia and industry to assess the opportunities, challenges, and prospects of achieving the holy grail of cancer research, a therapeutic approach for the ~30 percent of human cancers that are RAS-mutant.

After participating in this CME activity, physicians should be able to:

  • Compare therapeutic strategies being developed that target several RAS effector pathways, impact membrane targeting of RAS, and regulate RAS function;
  • Identify models of RAS-driven cancers including the role of the inflammatory microenvironment and signaling pathways in oncogenesis;
  • Explain the role of systems biology and functional genomics in the understanding and development of targeted approaches to RAS-mutant cancers;
  • Articulate the challenges and opportunities in developing effective therapeutic approaches for RAS-mutant cancers; and
  • Distinguish between RAS subtype-selective targets and approaches to targeting RAS, including the development of KRAS inhibitors and the role of post-translational modification.

DISCLOSURE STATEMENT

It is the policy of the AACR that the information presented at AACR CME activities will be unbiased and based on scientific evidence. To help participants make judgments about the presence of bias, the AACR will provide information that Program Committee members and speakers have disclosed about financial relationships they have with commercial entities that produce or market products or services related to the content of this CME activity. This disclosure information will be made available in the Program/Proceedings of this conference.

ACKNOWLEDGEMENT OF FINANCIAL OR OTHER SUPPORT

This activity is supported by grants and will be disclosed at the activity.

QUESTIONS ABOUT CME?

Please contact the Office of CME at 215-440-9300 or cme@aacr.org.